Ahmad Can't Run

Muscle Weakness
1. Causes of muscle weakness
  1. Infection
    1. poliovirus > poliomylitis
    2. Lyme disease
  2. Neurological
    1. Demyelinating disorders
      1. Guillain-Barré syndrome
  3. Medications
    1. Statin> atorvastatin (Lipitor)
    2. Amiodarone (oral route)
  4. Electrolyte: Hyperkalemia
  5. Genetics
    1. Duchenne muscular dystrophy
      1. DMD Gene
        Found on xp21
        2.2 megabases
        79 exons
        8 promoters
        Introns make up 99.4% of the entire gene.
        Mutations
        60% are deletions
        5-10% duplications
        30% point / splice site modifications
        encodes for the protein dystrophin, found in muscle cells and some neurons.
        Dystrophin provides strength to muscle cells by linking the internal cytoskeleton to the surface membrane.
        Without this structural support, the cell membrane becomes permeable.
        In DMD the damage to muscle cells is so extreme that the supply of stem cells are exhausted and repair can no longer occur.
      2. DMD is a sever progressive X-linked inherited disease characterized by progressive degeneration of the skeletal muscle especially those of the shoulder and pelvic griddle.
        clinical features
        Progressive weakness
        Intellectual impairment
        Hypertrophy of the calves
        Proliferation of connective tissue in muscle
        A mutation in the gene encoding for dystrophin protein, which is Xp21 gene.
        Due to loss of dystrophin
        1-fragile sarcolemma
        Which leads to
        1-increased osmotic fragility of dystrophic muscles
        2-exceesive influx of calcium ions
        3-release of soluble muscle enzymes such as Creatine kinase.
        4-Necrosis of the muscle cell.
        Pathological progression
        2-loss of interaction between the sarcolemma and extracellular matrix.
        3-separation of the sarcolemma from the basal lamina.
        Which leads to
        Difference between BMD and DMD
        BMD is milder and has low levels of dystrophin due to
        Clinical progression
        1-Early
        Infancy Poor head control
        2-Transitional
        Toddler
        hip weakness and lordosis
        3-9 years
        Gower sign and HT of calf.
        3-Loss of Ambulatory
        10-14 years
        Wheel chair
        4-Late
        +15 years
        Respiratory-cardiac-CNS complications
        Complications of DMD
        Cardiac
        Arrhythmias
        -Cardiomyopathy
        Orthopaedic problems
        -Joint contractures
        -Osteopenia –because of immobility but also secondary to steroid treatment
        -Scoliosis
        Infectious
        Pulmonary infections
        Pulmonary
        Respiratory insufficiency with decreased total lung capacity, decreased residual lung volume
        With an incidence of one in 5,000 boys, which are 200 per million births.
      3. Investigations
        Serum Creatine Kinase
        used to detect i (myositis) or (myopathies) such as muscular dystrophy
        A high CK generally indicates that there has been some recent muscle damage but will not indicate its location or cause.
        to detect if Ahmad has any muscular disorder since he already had muscle weakness and pain.
        Electromyography
        is a diagnostic procedure to assess the health of muscles and the nerve cells that control them (motor neurons).
        EMG translates electrical signals of our muscles into graphs, sounds or numerical values
        The doctor has ordered electromyography because Ahmad was complaining of muscle tenderness and weakness.
        Thyroid Function Test
        blood tests that determine the function of the thyroid gland
        by measuring : TSH , thyroid-stimulating hormone (TSH) thyroid hormone levels, thyroxine (T4) and triiodothyronine (T3)
        Since Ahmad had muscle weakness, the doctor wanted to check thyroid hormones levels since they affect many conditions in our bodies including muscle strength
        Western Blot
        to detect and analyze proteins
        Since the doctor was suspecting DMD, he wanted to make sure that the dystrophin enzyme is absent .Compared it with BMD to see how BMD is a milder form that has low dystrophin
        Muscle Biopsy
        Shows myopathic changes such as; connective tissue proliferation, scattered degenerating and regenerating myofibres
      4. Management
        Pharmacological
        Corticosteroids such as prednisone, can help improve muscle strength
        Heart medications, such as angiotensin-converting enzyme (ACE) inhibitors or beta blockers, if muscular dystrophy damages the heart.
        For controlling the asthma exacerbation Albuterol is used.
        Non pharmcological
        Physical and occupational therapy
        Gene therapy
        Stem cell
      5. Prognosis
        death occurs usually at about 18-20yrs of age
        The causes of death
        Respiratory failure
        Heart failure
        Pneumonia
        Aspiration
        Airway obstruction.
        dystrophy leads to progressively worsening disability
  6. Metabolic
    1. Glycogenoses: Acid maltase deficiency
2. History taking for muscle weakness
  1. Introduction
    1. Greeting the patient, insure privacy
  2. Duration &Location
  3. progression
  4. Radiation
  5. Quality (Pain Scales /questionnaire) & Quantity
  6. Aggravating factors &Alleviating factors
  7. Associated symptoms
  8. History of medication
  9. Family history
  10. Muscle Strength Scale
3. Neurological Examination of lower limb
  1. Motor system
    1. Fasciculations and muscle wasting
    2. Tone
    3. Clonus
    4. Power at hip, knee, ankle, and tarsal joints
    5. Coordination
      1. Heel–shin test
      2. Toe–finger test
  2. Sensory System
    1. Dermatomes
    2. The superficial or cutaneous reflexes
  3. Gait
    1. Gait Cycle
      1. stance phase
        begins with heel strike and ends with push off from the forefoot
      2. swing phase
        begins after push off when the toes leave the ground and ends with the heel strike.
      3. Abnormalities
        inadequate abductor muscles of the hip.
        Lateral trunk bending (Trendelenburg gait, gluteus medius gait.)
        Forward flexion of the trunk early in the stance phase. Compensates for inadequacy of the knee extensors.
        Anterior trunk bending
        Backward movement of the trunk early in the stance phase. Compensates for inadequacy of hip extensors.
        Posterior trunk bending (Gluteus maximus (Lurch) gait)
        The legs are not different in length when measured but are unable to adjust to the appropriate length during the gait cycle.
        The long limb is circumducted during the swing phase. Circumduction may also be used to advance the swinging leg in the presence of weak hip flexors
        Swing-out gait (circumduction gait)
        The pelvis is lifted on the side of the swinging leg (normal) by contraction of the spinal muscles and the lateral abdominal wall.
        Hip hiking
        Exaggerated hip and knee flexion to lift the foot higher than usual for increased ground clearance.
        Steppage gait
        Going up on the toes of the stance phase leg. Results in exaggerated upward movement of the trunk. Seen in Weak hamstring
        Vaulting
        A rhythmic disturbance in which as short a time is possible is spent on the painful limb, and a correspondingly longer time is spent on the pain-free side.
        Antalgic gait
        In parkinsonism
        Shuffling gait
        A rhythmic disturbance where the timing alters from one step to the next. Also occurs in drunk people.
        Ataxic gait
Foot and ankle joint
1. Foot Anatomy
  1. Muscles
    1. Layer 1
    2. Layer 2
    3. Layer 3
    4. Layer 4
    5. Muscle Development nutrients
      1. Calcium
      2. Iron
      3. Vitamin D
      4. Magnesium
      5. Vitamin B12
      6. Zine
      7. Omega 3
      8. Vitamin C
      9. Vitamin B1
      10. Proteins
  2. Arteries
  3. Nerves
    1. sensory nerve supply of the foot
  4. Ligaments
  5. Ankle Joint
  6. Bones
2. Physical examination for
  1. Introduction & Consent
    1. HEPA
  2. Inspection
    1. Palpation
      1. Skin Temperature Joints Tendons Ligaments
      2. Move
        Dorsiflexion
        Plantar Flexion
        Inversion
        Eversion
        flexion of the great toe
        special tests
        Inversion and Eversion stress test
        Thompson’s test
        for tendoachillies rupture
        Tests for Morton’s metatarsalgia
        Inspect the footwear
        Test Gait
        Drapes the patient
        DR.TH
    2. SSSP

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Ahmad Can't Run

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	Criado por Fatma Shwaylia mais de 7 anos atrás